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poisonous
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8/10/2019 Manual of Poisonous Plants
36/180
CHAPTKR
IV
FORAGE
POISONING, ERGOTISM,
AND
ASPERGIUOSIS
We have
several excellent illustrations
of
how
other
Forage Poisoning external known parasitic organisms
may
produce
disease.
Catarrhal stomatitis, for instance, may be
produced
by
the
ingestion of fodder
which
has become infected
with
any
one of
several fungi
belonging
to
distinct
orders.
Among
these
are the
rust
of
clover, bacteria,
mil-
dew
of
grass,
and
the rape-destroying fungus, Polydesmus exitiosus;
even the
common grass
rust
and other rusts
upon
grasses
as
well
as
the bunts-
and
smuts
are known
to
produce
this
form
of disease. Among higher
plants, such products
as
the
pungent
spices of
pepper
and
of the
roots
of
horseradish
and radish are
treated at length in such pathologies as the Friedburger and Frohner Veterinary
Pathology.
Serious diseases
of the
stomach
are
caused not
only
by
pathogenic
germs
but also
by the
ingestion
of various foods. Many
foods,
such as unclean, or
damaged
fodder, poor
water,
musty hay,
mouldy
corn, decomposing potatoes, are
responsible
for
gastro-intestinal
catarrh;
many
fodders,
also, contain
irritant
substances. There
are
several
forms of
gastro
enteritis.
Among forms of the
third class
(including
those caused
by
ingestion
of lower organisms such
as
fungi
or
poisonous
substances)
we
may mention
botulism,
fish poisoning,
injuries
produced
by
mould fungi, smuts, rusts, and,
finally,
the
so-called
toxic
gastro-enteritis
produced by
numerous
poisons.
These
have sometimes been
classed
as
irritant
poisons and narcotic
irritant poisons.
The
vegetable
poisons
under
this head are
numerous and have been treated
under the
different
plants.
Some
pathologists, however, mention
especially
lupinosis
of
sheep
and
equisetosis.
The
terms
applied
to
this
disease
are
Cryptogamic
Poisoning,
Forage
Poison-
ing,
Enzootic
Cerebritis, Epizootic
Cerebro-Spinal
Meningitis,
.Leuco-Encaphali-
tis,
etc.
Characterization. So-called forage poisoning
among
horses
and
mules
is a
non-communicable
disease, which
undoubtedly
belongs
to
a
group
of cryptogamic
poisonings. Horses seem
to
be
slightly
more
susceptible than
mules,
although
it usually
terminates fatally in
both
species.
The disease is
characterized
by
symptoms
which are
referable
to
a disturb-
ance
in the
central
nervous system, and
by
lesions
which,
if present,
are
also
found
there.
The
course of the disease
may
be
very
acute,
or
it
may
be
greatly
lengthened,
depending upon
the
suddenness
of the
onset.
The
mortality
is
very high
and
but
few
well developed
cases
ever recover.
Suckling
foals
do
not
contract
the disease.
History.
This
disease
has
prevailed quite
generally
throughout
the
Eastern
and
Central parts
of the
United
States
for
many
years,
but
until
recently has
not attracted
any considerable
attention.
During
the
past
few years,
however, it
has
occurred
with
unusual
frequency
in the
Central
West,
and, because
of
the
extensive
losses
directly
attributable
to
it,
has
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FORAGE
POISONING
ERGOTISM
21
become
of great
economic
importance.
In various
parts
of Iowa,
for instance,
individual
stock-owners
have
lost
several
thousand dollars
from
its
ravages.
In the
different
localities the
disease
has
been
known
by various names,
such
as
grass
staggers,
choking
distemper,
and
putrid
sore
throat,
and
because
it
apparently
presents
some
of
the distinguishing
characters
of a
specific infec-
tious
disease,
has
been
frequently
recognized
as infectious cerebro-spinal
meningitis.
A
noteworthy
fact
however
is,
that
thus far no
evidence
has been
discovered
which
would
indicate that
the disease
is transmissable
from animal
to
animal,
or
that
it
is
even inoculable.
On the
other
hand,
an
outstanding
feature
in every
outbreak is, that the
affected
animals
have had
access
to unwholesome
food, either
while
at
pasture
or in
the stable.
Fig.
3.
Common
Aspergillus on
mouldy
corn.
1. General appearance, showing
long
conidiophore
and
sterigmataj
on end.
2. Perithecium
with one of
its asci
and
ascospores.
3. Contents
from an
unripe
perithecium. 4. A
small
part
of
the mycelium
with conidio-
phore c and
spore
bearing sterigmata;
young ascogonium
as.
2, 3,
4 after DeBary.
Geographical
distribution.
The
disease
has been
reported
from nearly
every
part
of
the United
States.
It
never
becomes
epizootic, but is
usually
confined
to
isolated
localities.
While forage
poisoning
is
not
necessarily peculiar
to low,
poorly drained
districts, it
is
at
least most
frequently
observed
in
those
places
where
conditions
are
most favorable
for
the
development
of
cryptogamic
growth.
Etiology.
The
disease
seems
especially likely
to appear
when
horses
or mules are
fed on grain or
fodder
which
has
become overgrown with
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22
MANUAL
OF
POISONOUS
PLANTS
moulds, or when at
pasture,
they have had
access
to
grass
which, for
various reasons, has
become
fermented
or
mouldy.
Various
micro-organisms
have
been found to
be
associated with the
disease,
but
as yet
none
have
been
proven
to
possess
any
etiological
significance.
Cultural
and
histological studies
have
all
proved
negative.
Dr. Moore has in
one
instance
succeeded
in obtaining
a pure culture of
the colon bacillus from
the
brain.
oymptoms.
Depending upon the
severity
of
the
attacK,
tne
aisease
inay
manifest itself in any one
of
three
forms,
namely; acute,
subacute
and
abortive.
It
is
possible to
observe all
of these
forms
in a
single outbreak,
as the sudden-
ness
of
the onset is apparently regulated by
the amount of
the
poison
laden
food which the
animal
has
ingested.
The
acute
type is
characterized by
the abruptness of
its
appearance,
and
the
grave general
disturbances
which
immediately
manifest
themselves.
There
is
sometimes
violent
trembling
and
twitching
of
the
muscles
over
the
entire
body,
but most commonly the acute
form is
ushered
in by stupor.
There
is
manifested
a
weak,
staggering gait
and the
pharynx
is
either
partially or
completely
paralyzed. The tongue
may
also be
partially
paralyzed
and protrude from the mouth, and saliva falls in
strings
from
the
lips. The
pupil
is
dilated
and
the conjunctiva is,
as
a
rule, highly congested. The pulse
is
variable
and may
be
very rapid and hard, or
scarcely
perceptible; the respira-
tion is hurried
and
jerky.
The
temperature may
be
slightly
elevated,
but is
most
frequently
subnormal. Intestines
and
bladder are
paralyzed.
In this
form there may
be slight muscular rigidity affecting the muscles
of the
back,
neck and jaws, although in
many
cases this symptom never
mani-
fests
itself.
There
is
no rigidity
of
the ocular muscles.
The
animal soon
becomes so
weak that
he is no
longer
able
to
support himself and
falls.
Delirium
may manifest
itself, in
which the patient
may perform
a
series
of movements as
if
trotting, or
become so
violent
as to do himself serious injury,
but most
often
coma and complete
paralysis
supervene
and
death
results
in
from four
hours to two
days
from
the commencement
of the
attack.
The
subacute form is much the same
as the preceding, except
that it
developes
more
slowly
and
the
symptoms
are not
so
violent.
It is first
noticed
by
a
slowness
in
mastication
and
a
difficulty
in
swallowing.
A
further
indication
of approaching
paralysis
is seen in the
frequent
knuckling
and
the
loss
of
control over the tail.
The temperature
is
subnormal
and
the
pulse
and
respira-
tion are but
slightly altered.
The bowels
and
bladder are
inactive and
it
is
seldom
that
voidance
of urine
and
faeces
occurs
voluntarily.
There is
but
slight
rigidity
of the
muscles
if
indeed
there is
any,
and
no
evidence
of
pain
is
apparent.
These
symptoms
may
last
two
or
three
days,
when
gradual
improve-
ment
takes place,
or
the paralysis
becomes more
complete,
the general
weakness
more marked, paroxyms
of
delirium
develop, with
inability
to stand,
breathing
becomes
more
labored,
coma
comes
on and
death
results
apparently
without
a
struggle.
This form lasts
from
six
days
to two weeks.
In the abortive
form
there
are no well marked
constitutional
symptoms.
The
appetite
may
be
somewhat
lessened, the ability
to
swallow
slightly
impaired,
and the animal's
movements
a little uncertain,
but
no
very
noticeable
symptoms
appear
to
attract
the attention.
Improvement
usually
takes
place
on the
third
or
fourth
day, and
recovery
is the
usual
result.
Lesions.
As
a rule,
post-mortem
examination
reveals
no
naked
eye
changes
in
the
tissues
of animals
dead
of
forage
poisoning.
There
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FORAGE
POISONING ERGOTISM 23
may
be congestion
of the
brain
and cord with extensive
effusion
into the
ventricles
and
subarachnoid
spaces. Few
small
hemorrhages and
parenchyma-
tous
degenerations
within the
various organs
have
been
mentioned.
MacCallum
and
Buckley
have
found
in the
brains
of
horses
dying
of
this disease, areas of
softening
in
the
frontal region
on
each side, anterior to the
motor region
of
the
cortex.
This
lesion
was
practically
confined to
the
white matter
immediately
under
the
cortex. In the affected
areas
there
was
complete
destruction of
the
brain
substance,
in
which the
anatomical structures are disintegrated and largely
replaced
by
a
colloid-like material.
The neighboring
blood
vessels
were
acutely
inflamed,
with
cellular infiltration
of
leucocytes
and
red
corpuscles into the
perivascular
spaces and tissues.
In a later outbreak
these
writers
failed
to
find
the
brain lesion, but did
observe the
vascular
changes
above
described.
McCarthy and
Ravenel,
in a study of fifteen animals found certain lesions
in
the upper gastro intestinal
tract
and in the
central
nervous system.
These
were:
(1)
In
the intervertebral
and
Gasserian ganglia, where a pericapsular,
small round
cell
accumulation was
present.
The cells were all of the
same type,
the nucleus
and
protoplasm
being
about
the size
of
a red
corpuscle.
There
was
no
evidence
that
these
cells were the
result of
proliferation
of the
original
layer of capsular
cells.
(2)
Cortical lesions.
These
consisted
of congestion of the cerebellar
and
cerebral
cortex.
There
were
also capillary
hemorrhages.
The
meninges
were
normal.
(3)
Changes in the
choroid plexus.
In
three cases
the
choroid plexus
was
changed into
a
triangular
tumor-like mass,
of a yellowish red color
and
of
a
firm consistency.
The
increase
in
size
was
found to be
due to
a
proliferation
of
the
elastic tissue
surrounding
the
vessels.
(4)
Changes in the nerves.
There
was a
distinct
degeneration of
the
nerves
supplying the
larynx and neck.
This
was
present in the nerve
up
to
the
ganglion, but
was
not
found
in the posterior
roots.
Other slight
changes
were
detected.
Moore
failed to find any
gross
lesions in the
nervous system
and other
organs
in
the
cases
examined
by him. In one
case
the brain,
spinal
cord, and
organs
were
studied
histologically
with negative
results.
Differential
diagnosis.
A very
important
point
in the recognition of
forage-
poisoning
is the history which has been referred
to
previously.
It
must be
distinguished
from inflammations of the brain and
meninges,
and
from
rabies.
Treatment.
In the acute
cases
this is seldom
successful,
although
quick-
acting stimulants
to arouse
the
patient may
be
tried.
In
the
subacute
cases
a
purge should always
be
given
to
rid the
intestines
of the
poison. Strychnin in
large
doses,
to
overcome the extreme
depression
of
the
nerve
centres,
and
atropin
to
support
a
failing
circulation
may
be administered
hypodermically
at
frequent
intervals
with benefit.
In the
very mild
cases,
all that is
necessary
is
to
empty
the bowels
with
a
purge.
It
is
of
the utmost
importance, in
all
cases,
with the
return
of the
appetite,
to
supply
only
such
food and
water
concerning the
wholesomeness
of
which
there can be
no
question.
Prevention.
Since
it seems
to
be
quite
generally
accepted that this
disease
is
brought about
by
the
ingestion
of
mould-contaminated
food
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24
MANUAL
OF POISONOUS
PLANTS
the prophylaxis is
apparent. Whenever
the
disease
makes
its
appear-
ance
either in a stable
or
a
pasture, the
animals
should
be
immediately
removed
from further
exposure
by
changing
the
food supply.
The
food
should
come,
preferably, from a
clean,
new source and the
water
should
not
be
contaminated
by surface
drainage.
It
is also
well
to
thoroughly
disinfect
the
mangers
and
feed-boxes,
and
render inocuous the
soiled
litter.
There is no
known means
of artificial
protection,
and
the
disease
will
recur
if the
animals are
again allowed access to
spoiled
food.
(Stuhr).
History.
During
the
winter of
1908-1909,
several
cases of
Poisoning from
pQJgQ^jjjg
from
spoiled silage
were
reported
to
Dr. Stange of
Silage
jj^g lo^N^. State
College.
Other cases
have
no
doubt
been en-
countered. In every instance,
as
in the
case
reported by
Dr.
Beaumont,
below,
moulds occurred
in
the silage. Dr.
Beaumont says:
I
am
sending
you under
separate
cover
by
a
specimen
of
corn
silage
upon
which
you
will
notice
is
growing
some
form
of mould
which in my opinion
is
accountable
for a
very
peculiar
disease,
existing
among
a
herd of
young
horses
and
mules
belonging
to a
farmer
living here.
Dr.
R.
E.
Buchanan found these moulds
occurring in
spoiled
silage
to
be a
species
of Monascus. Other moulds, Mucor,
Penicillium
glaucum, and Verticil-
Hum
were also
present;
but there
was
a
preponderance of
Monascus.
Symptoms.
The first animal,
a
three
year
old
filly, was
taken
sick about
April 1st, showing symptoms as follows:
Gaunt, depressed,
stiffness
of
gait.
When lying
was
unable
to rise, but
when
assisted
to
rise
would stand and show
inclination
to
eat
but
was
unable
to
masticate and
swallow
food.
Temp.
103.5
F. Pulse
86,
Respiration
36;
friction sounds
distinctly
heard
at each
heart
beat.
A whistling
sound was
emitted during expiration
and
there
was
also a
suppressed
painful
cough.
Animal
died
in
about five
days.
A
two-year-old mule
and
one two-year-old
filly
were attacked with disease.
The
mule
is
improving
and
will
recover
but the
two-year-old filly
shows exactly
the
same
symptoms
as
Case
No.
1,
aside
from being especially stiff
and
lame
in
one
fore shoulder,
and I think will die within
two days.
Treatment. The
treatment
as
followed
by
Dr.
Beaumont
is
described in
detail
in
his
paper before
the
Missouri
Valley
Veterinary
Association,
June
16-17, 1909. Briefly, the method
was
as
follows:
Tincture Strophanthus
in two-dram
doses, every
two
hours
(given as a
cardiac stimulant, the heart action
being
very
weak). 1 quart of raw
linseed
oil
given in
two
doses, six hours
apart (as
general
laxative).
Potasii
Nitras
in half to one ounce doses, dissolved in
water and
given as
a drench, every
three hours
(alterative
diuretic, and
respiratory
stimulant).
After
the
first
twenty-four
hours the Tr.
Strophanthus was
discontinued
and
he began giving
Iron Quinine and Strychnin tonic in one-ounce
doses
three
times
daily.
This
was
continued with the
Potasii Nitras until the animal
showed
marked im-
provement
when
both remedies
were
discontinued
and
he
prescribed
Fowler's
Solution
(Liquor
Potasii
Arsenitis)
in half-ounce
doses three
times
daily
during
convalescing
stage
of the
disease
which
lasted
about
ten days or two
weeks.
Dr.
C.
H.
Stange
has contributed the
following
on
forage poisoning
and
especially
with reference
to
silage:
Numerous
cases have
been reported
of
an affection
of
the
central
nervous
system, the symptoms
being
in general quite similar
but
different
and
varying
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FORAGE
POISONING
ERGOTISM
25
causes
are
assigned.
Dr.
Francis
reports
that
in the fall of
'03,
spring
of
'04,
four
to five
thousand
horses
and
mules
died
with
a
nervous disorder
character-
ized
by
structural
changes
in the
brain
which
cause
incoordination, delirium,
coma
and
usually
death.
He
concludes
that the disease
is
not
caused
by
moulds
but
is
the
result of
animals
having
free
access
to
a labor diet
when
kept
in
idleness.
He was
unable
to find
the germ
described
by
Wilson and Brimball.
Professor
Harrison
of the
Ontario
Agricultural
College reported several
cases
and
as a
result of his
investigations
he
concluded that
the
disease
was
due
to a coccus insolated
from
the meningeal
fluids.
Pearson studied
an out-
break
in
seven
horses,
five
of
which
died.
The
outbreak
occurred soon after
opening
a
new silo,
the
ensilage
from which was
mouldy.
The
symptoms
ob-
served
were
very similar
to those
observed by
Professor
Harrison
and
he
emphasized
the
paralysis
of
the pharynx
and
great
muscular
weakness. He
concluded
as
a
result
of feeding
experiments
that
the
so-called
cerebro-spinal
meningitis
was
a
forage
poisoning.
Dr. Dow of
Connecticut
describes two
cases which were
attributed
to
watering
from
a
tub containing
a
mouldy
slime.
Dr.
Ferguson
of
Texas describes three cases of forage
poisoning
due
to
smutted
corn. There
was
vertigo,
coma, low temperature,
pulse
in later
stages
rapid
and
irregular.
In 1901
Dr. Hickman
investigated
an outbreak
among horses
in North Carolina
in which a large number of horses died.
In 1906
another
outbreak occurred
at the same place
(Hyde
Co.)
in
which
about
forty
horses
and
mules died in about three
weeks.
The
cause in
these
cases seemed
to
be
moulds
on
vegetation.
On
the
whole
the
country
is
low
and swampy.
The
pathological
changes of
Epizootic
Leuco-Encaphalitis were described
by
McCal-
lum and Buckley
in
1902. Muller
of
Germany
reported
an outbreak
among
horses, cattle
and
sheep
due to mouldy straw. (Berliner-Tierarztliche
Wochen-
schrift). Drs.
McCarrol and
McMullen
describe an
outbreak
of
cryptogamic
poisoning in horses due to feeding mouldy
beet
tops.
Dr.
Eockhart
describes
several cases
in Canada. The prominent
symptom
seemed
to be
the
inability
to
swallow.
Two
outbreaks have
come
under our
observation
during the past year.
The first consisted of eleven head of
horses, two
horses were being fed for
market,
the others
were
fed
in
the
same
manner during
the nights and turned
out
during
the day. The first
animal
affected was
one
being fed for market.
It
ate part
of
its
feed
in
the morning
but
in
a
few
hours
showed symptoms of
ptyalism,
depression
and
paresis of
the
hind
quarters.
By
noon
the
animal
was
down, unable
to
rise and
struggling
some,
and
died that
night. The
next
animal to show symptoms was its
mate.
The
symptoms
shown in this case
were
similar
to acute cases
of
the so-called cerebro-spinal meningitis, coming on
with
trembling
and
weakness
causing
the
animal
to stagger.
An early symptom
in
all
cases
coming tinder
our
observation
is the
ptyalism
due
to
inability
to
swallow. (Dyspagia).
As
a
result
the
saliva collects
in
the
mouth
and
hangs
from
it
in
strings. Muscles
of
different
regions of the
body
are liable
to
con-
tract.
The
breathing
is
rapid and
in
some
cases
may be
of
the
Cheyne-Stokes
variety.
The
temperature
in
this
case
was
sub-normal. In
some
of the more
chronic
cases
and when the
animal has been down
for
some
time
with con-
siderable
struggling
the
temperature
was
somewhat
elevated. The
pulse was
variable,
being
about normal
in some cases
and
rapid
and
almost imperceptible
in
others.
The
animal became
quite
violent at times and finally
died living
but a
few
hours
longer
than
the
first
animal. The
other
seven
animals showed
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26
MANUAL
OF
POISONOUS
PLANTS
a
more chronic
course, showing
inability
to
swallow,
slow,
weak
pulse, difficult,
noisy
respiration,
weakness
and
paralysis,
spasm
of
muscles
of head,
neck
and back,
death taking
place in
from
two
to six
days.
The
other
two
animals
showed
a mild type
of the
disease
as
slight
loss
of
control,
some
exophthalmia,
loss
of
appetite
and thirst
and loss of
condition.
These
animals
were placed
on potassium
iodid
and nux
vomica
and
recovered.
This outbreak was
attributed
to
mouldy silage,
which
was
being
fed
to
the
horses,
but in
order
to
be
more
certain ISO pounds
of
silage
were
ship-
ped
to
the
college
and
fed, first
to
one horse
which died in two
days
from
an
acute form
of
the disease.
Another
horse was fed but
would not
eat
the
silage
so
well, consequently did not die quite
so soon,
living
for several
days.
In
both
cases
the
symptoms
resembled those seen in the
original
outbreak.
Post mortem
revealed
no
changes except a few
petechia along
the
small
in-
testine,
a
few
infarcts
in
the
kidney
and
slight
softening
of
the
brain.
This
however
was
not
very
marked,
probably due to
the
fact
that
they were
acute
cases. Microscopic examination revealed the
presence
of
mould
in the
mucosa
and submucosa of the intestine, also mycelial
threads growing
between
and
around the
renal
tubules.
The other outbreak consisted
of
four horses, three
of
which died
of
an
acute form of
the disease, the
symptoms being
similar
to
those already
des-
cribed.
The
fourth
being
of a
more chronic
nature
was placed
on potassium
iodid
and
nux vomica and
recovered.
In this outbreak the
hay
was
found
to
contain
a
fine
mould
and was
cut
from
an
old
pond
which
had
been
plowed
up
and
seeded.
The
water had
overflown this, however,
and
stood for
some
time.
The
symptoms
and
post
mortems
were
similar
to those
described in
the
first outbreak, with the exception
that
no
histological examinations
were
made.
A
form of
cerebro
spinal
meningitis
is
quite
common in Germany.
It has
also been described in
Australia, Great Britain and
Russia.
It may
be
that
these
outbreaks are
due
to other
causes
than those
already
described.
Sid-
amgrotzky
and
Schlegel
found a form
of
coccus in
the
sub-arachnoid
fluid,
but
it
was necessary
to
make
sub-dural
injections of cultures
of
this
organism
to
cause
meningo encephalitis.
Johne
found
a diplococcys
in
the cerebro-spinal
fluid of affected
horses.
Ostertag
found
a
diplococcus
similar to the
one
found
by
Johne
in the
cerebro-spinal
fluid in the so-called
Borna's
disease. They
were
pathogenic for
horses and
sub
dural injections produced
symptoms
and
death
similar
to
cases
of
Borna's
disease.
Hutyra and
Marek call
attention
to
the fact
that bacter-
iological investigations have
not
been
followed
by the
same
result but possibly
the
several investigators
were
working
with the same
organism.
Nevertheless
it remains
to
be shown whether all
cases of
cerebro-spinal
meningitis
are
due
to the
same
cause and
resemble
Borna's disease.
On
the
other
hand
it
is
possi-
ble that
epizootic
cerebro-spinal
meningitis
of
domestic
animals
has
no
specific
cause.
It
is apparent
that
mouldy
food
and
water
has
caused
several
outbreaks
in
this
country.
Natural
infection
in European
outbreaks
is
also
supposed to
take
place
through
infected
food
and
drinking
water.
The
disease
is
not trans-
mitted from
one
animal
to another.
Mohler calls
attention
to
the
very inter-
esting work of
Schlegel
and the Berliner
Tierarztliche
Wochenschrift
who
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FORAGE
POISONING
ERGOTISM
27
ERGOT
ON
VARIOUS
GRASSES
FiB.
41.
Manna
Grass {Glyceria nervata). 2. Blue Grass
(Poo).
3.
Spikelet
of Bottle
Crass iAsprella
Hystrix). 4. Reed Canary Grass
(Phalaris
Arundmacea).
5.
Wild Rye
(Ely-
mus
robustus).
6.
Koeleria. cristata.
7.
Wheat
Grass {Agropyron
Smiihii).
8.
Red Top
(.Agrostis
alba).
9. Blue
Joint
(.Calamagrostis
canadensis).
10.
Timothy
(Phleum
pratense).
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MANUAL OF
POISONOUS
PLANTS
associates with
the affection an
organism which
he
termed
Streptococcus
mel-
anogenes. Mohler
states,
however,
that
whether the
disease
is
of
microbian
origin or an
intoxication has not yet
been
definitely
established.
Ergotism
is a disease
of bovines
caused
by
the
ingestion
of
Ergotism considerable
quantities
of
food
contaminated
by
ergot.
Equines
are
apparently less
susceptible than
bovines,
although
the
horses
have
been
known
to
suffer severely
from the
disease.
Ergotism
in man is
not
an
uncommon occurrence, and in
nearly
every
instance
it
has
resulted from
eating
bread
made
of
ergotized
grain.
The disease
makes
its
appearance among
cattle chiefly in
the winter
and
spring
seasons
and
has at
times been
the
cause
of
serious
losses
throughout
the
central
and
western states.
Ergot is the
sclerotium
of
a
parasitic
fungus, Claviceps
purpurea, which
infests many
species of
native
and
cultivated grasses, and
appears on some
of
our
grains, especially
rye.
The
sclerotium
represents
a
stage
in
the
life
history
of
the fungus, which is intermediate between that of the
mycelium or
spawn,
and
that of
the
spore-bearing
thallus. It
flourishes
particularly
well on rich
soil
and
in
warm, damp
seasons.
The chemistry
of ergot is
not
exactly known,
although
Robert
succeeded in separating
three
bodies;
namely,
ergotinic acid,
cornutin,
and sphacelinic acid.
Ergotinic
acid is a
protoplasmic
poison,
and
when injected
intravenously
produces
inflammation
of
serous and
mucous
membranes,
disintegration
of
red
blood
cells, and
wide-spread
ecchymoses; cornutin
excites the
central
nervous
system
and
causes general convulsions;
and
sphacelinic
acid
induces
gangrene.
Symptoms.
Ergotism manifests
itself among
animals
chiefly in
the
chronic
form, since,
as
a
rule,
the poison
is
acquired
in
small
amounts and accumulation
takes
place slowly.
Two distinct
types
of
the
disease are recognized, namely:
spasmodic
and gangrenous.
Symptoms referable to the digestive
tract,
such
as nausea, vomiting,
colic,
diarrhoea
or
constipation
appear in
both forms.
Pregnant
animals
very frequently
abort.
In the
spasmodic
type of
the disease,
symptoms
due
to over stimulation
of the
central
nervous
system, appear.
These are
tonic
contraction
of
the
flexor
tendons
of the limbs,
anaesthesia
of the extremities,
muscular, trembling,
general
tetanic
spasm,
convulsions
and
delirium.
Death
usually
occurs
from
secondary
causes.
Gangrenous
ergotism
is attributed
to prolonged
constriction
of
the arterioles,
and more
directly
perhaps
to degenerative
changes
in the
vessel walls,
and the
consequent
formation
of
hyaline
thrombi.
It is
characterized
by
coldness
and
anaesthesia
of the
extremities, followed
ultimately
by
dry
gangrene
of
these
parts.
The
effects
of
this dry
gangrene
are often
very serious
and
amount
to sloughing
of the
feet,
tips
of
the ears,
tip
of the
tail, shedding
of the
hair,
teeth,
etc.
Death
takes
place
from exhaustion.
Lesions. With
the exception
of the
gangrene
which
may
vary
greatly
in
severity,
there
are
no lesions
of especial
significance.
Degenerative
changes
in the
sensory
area
of the
cord
and
in
the vessel
walls
have
been observed
in
animals
slowly
poisond
with
ergot.
Treatment.
The first
essential
in the
treatment
of
ergotism
is
to remove
the
cause.
In
well
established
cases
treatment
does
not
as
a
rule
prove
satisfactory.
Tannic acid
is
the chemical
antidote, and
should
be
given
to neutralize
the
unabsorbed
portion
of
the
poison.
Chloral
is
the
physiological
antidote.
In
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FORAGE
POISONING
ERGOTISM
29
addition
to
giving
the
antidote,
the
treatment
is entirely
symptomatic.
(Stuhr).
A
B
Fig.
5.
A. Aspergillus
fumigatus
showing
coniliophore
on
right
with sterigmata and
spores
attached
on
left. B.
A. niger
showing
conidiophore, sterigmata,
.and
spores
attached
in
chains.
After
Siebenmann.
Pneumonomycosis
is a not uncommon
disease
of
domestic
Aspergillosis
animals
caused chiefly
by
the mould,
Aspergillus
fumigatus,
although
the Aspergillus
niger is also
pathogenic for
birds. This
disease is
most frequent
in
birds, both
domestic and wild,
occasionally
observed
in horses
and
cattle,
and
rarely
in man. Respiratory
diseases
and
lowered
vital-
ity
predispose.
In all
species
the disease is
characterized
by purulent
local
inflammations in the lungs
or
other
tissues,
and
a
purulent
and necrotic
pseudo-
membrane
upon the bronchial,
tracheal,
and
other
mucous
membranes
upon
which it grows. The appearance
of
the pulmonary
lesions sometimes
resembles
tubercle,
sometimes
actinomycosis.
Pneumonomycosis
has been experimentally produced in birds
(pigeons
and
geese)
by
compelling them
to
inhale
aspergillus spores for
a
few minutes, after
which
they
usually die
of pneumonia
in
a
few days.
Rabbits
have
also
been
successfully inoculated
by
intravenous injection of spores.
Etiology.
In mammals the
Aspergillus
fumigatus
and in birds
the
Asper-
gillus fumigatus,
niger
and flavescens
seem
to be pathogenic
species.
Infection takes place most
commonly
by inhalation
of
the spores
which
often
are
suspended
in the air, or by taking them in with the food.
Intestinal
infection
has not
been
observed. The
spores are
widely
distributed
in
nature
and exist
in vegetable matter
and
grain
abundantly. They
possess
remarkable
vitality
and
exhibit
considerable
resistance
to
destructive agencies. The
patho-
genic
power
of
the mould
does
not
depend
upon
any product
which
it elaborates
but upon
the
reactions
which result
from its penetration
into
the tissues. Peck
observed
the disease
in seven subjects,
in
a
stable
where horses
were fed
on
mouldy
hacked
hay.
Symptoms.
The disease
is of slow
development
in
the
larger
animals and
may
not be
observed until
well
advanced.
In general the symptoms
are
of
a
pneumonic
nature
and in
addition
there
is
progressive
emaciation. A
case
in
a
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MANUAL OF POISONOUS PLANTS
Jersey
cow,
described
by
Pearson
and Ravenel
presented
the
following symp-
toms;
the animal
had
been
in poor condition
for
six
months
before it
was
examined.
It
was
weak
and depressed,
did not eat,
breathed
with
difficulty
and,
at
times,
coughed
violently.
Percussion of
the chest
gave
sounds
clearer
and
louder than
normal
and
auscultation
revealed
the
lung and
bronchial
sounds
much
intensified.
Six
days
later
these
symptoms became
more
pronounced,
the
respiration
and pulse
very rapid. The animal
gre*
rapidly
weaker and
died
ten days after first being
seen.
The symptoms
in
birds
are
much the
same as
those
in mammals except,
that
the disease
runs
a more
rapid
course.
Emacia-
tion advances
rapidly and
fetid diarrhoea may
set
in and
continue until
death
in from
a week to two
months. At
times
emaciation
is the
only
symptom.
Fowls
emit a glairy
discharge
from the nostrils which
may
contain
the spores.
In
the prevention of the disease
in
fowls therefore,
it is
necessary
to
isolate
or
destroy
the sick
fowls
together
with
the
carcasses
and
fumigate
the poultry
houses.
The roosts
may
be
whitewashed.
Lesions.
The
lesions take
the form of
a
miliary
suppurative process, the
foci
varying in size from very small up
to
that of a pea.
These
may
exist
in
large numbers
and
be scattered throughout the
entire lung.
Sometimes
they
become
confluent and
produce large areas
of
disease.
The
process
starts in
the
bronchial
mucous
membrane,
and
later involves the bronchioles
and alveoli.
A very important feature
is the
intense amount
of emphysema which
is
apparent
on
external
examination
of
the lung. The
lobules
are
often widely
separated
and
can
be
readily
seen
in
outline
when
a
portion
of
the
tissue
is
examined
by transmitted
light.
In
these emphysematous
interlobular
spaces,
and in the
air passages
are
seen
whitish, mouldy looking
patches. They
are
composed
of
denuded
epithelium,
inflammatory
exudate, fruit hyphae
and
spores.
The lesions
spread
by
penetration
of
the
mycelium
causing
a destruction
of tissue.
Spores
are not
found within
the
tissues. In rare
cases there is
diffuse
pneumonia
characterized
by
hepatization
and interstitial infiltration.
On
this
latter
account
the disease
has
been
described
as being similar
to
contagious
pleuro
pneumonia
of
cattle.
There
may
be
pulmonary
gangrene from
secondary
invasion
of putrefactive
organisms
acting
upon
the devitalized
tissue.
An
interesting
feature
is
that
this
disease
may
interfere
with
the
tuberculin
test.
This
was
shown in
the
case,
above
referred
to, in
which the test
was
used
without
success,
and
lesions
of
tuberculosis found
in
the lung
on
postmortem
examination.
Treatment.
This
must
of necessity
be unsatisfactory
since
it is
quite
impossible
to destroy the
moulds
which have
penetrated
the
lungs.
(Stuhr).
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CHAPTER
V
POISONING
FROM
FUNGI
That
fungi
of
various
kind
are injurious,
was known
to
the ancients,
trof.
Fordi
says,
The most interesting
cases
of
mushroom
or,
as
commonly
described,
toadstool
poisoning
and
one
of
the first
authentic
cases
on record,
occurred in the family
of
the
Greek
poet, Euripedes,
who lost
in
one
day, wife,
daughter,
and
two
sons,
who
in
the
poet's
absence
partook
of
the
deadly
species.
Among
the great
ones whose
lives
were sacrificed
to
the
same ignorance
may
be
mentioned
Pope
Clement VII.,
the Emperor
Jovian,
the
Emperor
Charles
VI.,
Berronill
of Naples and
the widow
of
Tsar Alexis. The
death of the Emperor
Claudius
is also assigned
to this cause,
but the
reason and manner
of
the
accident are
not
certain.
In addition
to
poisoning from
toadstools, it has long
been known that
Ergot {Claviceps purpurea)
is
injurious
to
man
and
lower animals.
In recent
years Ergotism
has
not been so serious
as
formerly.
Other
fungi
also
may
be
responsible
for
the
death of animals
by
poisoning.
The
Fly Agaric
(Amanita muscaria),
a
beautiful
species,
is common
in many
parts of the
United
States. I
have described
it
in detail in another part
of
this
work.
In
this
connection I
shall
quote
freely from the detailed and
excellent
account of poisoning
as
given
by
Prof.
V.
K. Chesnut,
and
the
excellent report
given
of A.
phalloides
by
Prof.
Ford, who
has
written
the most recent
account
of
poisoning
from this fungus.
The symptoms
and treatment are thus described
by
Mr.
V.
K.
Chesnut:
The
symptoms
of
poisoning
from the
fly
amanita,
as deduced from
a
number
of
cases, are
varied.
In some
instances
they
begin only after
several
hours,
but
usually in from one-half to
one
or
two
hours.
Vomiting and
diarrhoea
almost
always occur, with
a
pronounced
flow
of
saliva,
suppression
of the urine, and
various
cerebral phenomena
beginning
with giddiness, loss
of confidence
in one's
ability
to
make
ordinary movements,
and
derangement
of
vision.
This is
succeeded by
stupor, cold sweats,
and
a
very marked
weaken-
ing
of the heart's
action.
In case of
rapid
recovery the stupor is
short
and
usually
marked
with
mild
delirium. In fatal
cases
the stupor continues
from
one to
three
days and
death
at
last
ensues from
the gradual weakening and
final
stoppage
of
the heart's
action.
The
treatment for poisoning by
Amanita muscaria
consists
primarily
in
removing
the
unabsorbed portion
of
the
amanita
from
the
alimentary
canal and
in
counteracting
the
effect
of
muscarin on the
heart.
The action
of
this organ
should
be
fortified
at
once
by
the
subcutaneous
injection,
by a physician, of
atropin
in
doses of from one
one-hundredth
to one-fiftieth of
a
grain.
As
a
stimulant
emetic,
mustard
is
particularly
valuable.
If
this
is
not
effective
apomorphin
should be
administered by a
physician.
In
case
of
profound
stupor,
however,
even
this
may
not
produce
the
desired
action. Tannin
is of little
1
Science
N.
S.
.^0:
97,
98.
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32
MANUAL
OF
POISONOUS
PLANTS
or no
value
in
rendering
the muscarin insolu-
ble in the stomach.
If vomiting
has
not
taken
place, recently
burned
charcoal
or
two
grains
of
a one per cent
alkaline
solution
of perman-
ganate
of
potash
may
then be
administered,
in
order, in
the cases
of
the
former
substance,
to
absorb the poison,
or,
in
case
of
the
latter,
to
decompose
it.
This
should be
followed
by
oils and oleaginous
purgatives,
and the in-
testines
should
be
cleaned and
washed with
an
enema
of warm water
and
turpentine.
Experiments on
animals
poisoned
by
the
fly
amanita
and
with pure
muscarin
show very
clearly
that
when
the
heart
has
nearly
ceased
to
beat it may
be
stimulated
to
strong
action
almost instantly
by
the
use
of
atropin.
Its
use
as thus
demonstrated has been the
means
of
saving many
lives. We have in
this alkaloid
an almost
perfect
physiological
antidote
for
muscarin,
and
therefore in
such
cases
of
poi-
soning
its
use should
be
pushed as
heroically
as the
symptoms
will
warrant.
The presence
of phallin
in
Amanita
muscdria
is possible,
and
its
symptoms should
be
looked for
in
the
red
color
of
the blood
serum
discharged
from the
intestines.
Its
treatment,
which
is
difficult,
is
discussed under
Amanita
phalloides.
It is well
known
that in
some
parts of Europe the
fly
amanita, after the
removal of
the
poison
by
treatment
with
vinegar, is a
common
article of food.
It
was
interesting to
discover not long since that among
some of our own
people
a
similar
practice prevails. Though most
of
the colored women
of
the
markets
look
upon
the
species
with
horror,
one
of
them
recited
in detail
how
she
was
in the
habit of cooking
it.
She prepared the stem
by
scraping,
the
cap by
removing the
gills
and peeling
the upper surface.
Thus
dressed
the
mushrooms
were
first boiled in salt and water, and
afterwards
steeped
in
vinegar.
They were
then washed in
clear
water,
cooked
in gravy
like
ordinary
mushrooms
and
served
with
beefsteak. This
is an
exceedingly interesting
operation
from
the
fact
that
although
its
author
was
wholly
ignorant
of
the
chemistry of
mushroom
poisons, she had nevertheless
been
employing
a process
for the
removal
of
these
poisons
which
was
scientifically
correct.
The
gills,
according to
various
pharmacological
researches,
are
the
chief seat of the
poisonous
principles in
this plant
and
their removal
at
once takes
away
a
large
part
of
the poison. The
salt and water
would
remove phallin
or
any
other
toxalbumin
the
mushroom contained,
and although
the
presence
of
phalHn
or any of
this
class
of
poisons
has not been demonstrated
in
Amanita
muscaria,
there
is a
strong
suspicion
that it
may
occur
in slight
amount.
The vinegar,
secondly,
removes the alkaloid poison, muscarin,
and
the
mushroom
after
the
two
treatments
is
free
from
poisons. This
process
is
cited,
not
to recommend
its
wider
use,
but as a matter of
general
interest.
The
writer's
recommenda-
Fig.
6.
Deadly Amanita (.Am-
anita
thalloides).
U.
S.
Dept,
Agrl.
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POISONING
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33
tion
is
that a
mushroom containing
such
a
deadly
poison
should
not
be used
for
food in
any
form,
particularly
at a
season when
excellent
non-poisonous
species may
be had in abundance.
It
is
surprising
that
cases
of
poisoning
are
not
more
frequent.
At
Tacoma
Park, D.
C, on
November
9,
of last
year, a lady
who
has
a
thorough
knowl-
edge
of
edible
and poisonous
mushrooms met
a
family,
consisting of
a man,
woman,
and
two
children,
who
had just
completed
the gathering of
a basket-
ful
of the fly amanita and the
death
cup,
described
below,
which
they
were
taking home to
eat.
In
reply
to
questions the
woman
stated
that they
had
often
eaten
this kind
purchased
dry
at
an Italian
store,
but
that they
had
never
gathered fresh ones
before.
Of
course
they
had
mistaken
the
species,
or
pos-
sibly
the dried ones
were
fly
amanitas
from
which
the poison
had
been re-
moved by
treatment with
vinegar.
After considerable persuasion
the
people
consented
to
throw
the lot away.
Fiff.
7.
Fly
Agaric
(Amauila
muscaria).
U. S.
Dept, Ag.l.
It
is
impossible
to
say
what
amount
of the
fly amanita
would prove
fatal,
but
in
this
connection
it is of
interest
to
note the
custom
reported by
Krashen-
innikoff,
a
Russian
who travelled
in
Siberia
and
Kamchatka from
1733
to 1743,
namely
that
the
natives
of
the
latter
country,
particularly
the
Koraks,
used the
fly
amanita
as
an
intoxicant,
three
or
four
specimens
constituting a
moderate
dose
for
one
habituated
to
its
use,
but ten
being
required for
a
thorough
drunk.
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MANUAL
OF POISONOUS
PLANTS
The
same
observations,
with
varied
details,
have
been made
by
others,
par-
ticularly by
Langsdorff,
who
traveled around
the world with the Russian
navigator
Krusenstern
from 1803 to
1806,
and in
more
recent
times by Kennan
in his first
Siberian
journey
of
1865-67.
The
plant
may
be
taken fresh, but
its
taste is so
disagreeable
that
only
with
great
difficulty
can
a
sufficient
amount
be
eaten to
produce
the intoxicating
effect.
The
Koraks have two
principal methods of taking
it
:
First, by
swallow-
ing
pieces of the
dried caps without
chewing
them;
second,
by
boiling
the
dry
caps
in
water
anli then drinking the
liquor thus produced
mixed with
the juice
of
berries
or
herbs
to
disguise
the
taste. The
intensity
of
the poisonous^
character of the
fly
amanita
undoubtedly varies at different ages,
with
different
individuals, and
with
different
methods of
preparation.
The
amount of
the
poison
that can be
taken into the
system
with impunity
varies,
too,
with
the
person
who
takes
it.
The
fact
that
a
Korak,
who
has long
used
the
plant
as
an
intoxicant,
can
eat
ten
specimens and
merely
become drunk, does
not
prove
that
a
similar number would not
be
fatal to an
American
who
had never
eateri
it
before.
Very
diverse statements
concerning the properties
of
this
fungus
have
been
recorded. While some
have
attributed
to
it
edible
qualities,
others
have as-
serted that
it
is a most active poison and has
caused
numerous
accidents
by
being
confused
with the
Orange
amanita. It
is
said
to
have caused
death
even
when
eaten in small
quantities,
and
again
it is
said to
have
been
eaten
in
abundance
without
any
evil
results.
According
to
Quelet,
it
acts
as
a
cathartic
if
eaten
in
small
quantity,
but causes death
if
eaten freely.
One
of
my
own
correspondents
assures
me
that
he
has eaten
of
the
yellow variety, Var.
formosa,
without
evil
results,
and that
he
regards it as very good.
But
there
is no
disputing
the fact that the species possesses
intoxicating
and poisonous
prop-
erties. It has
long had
the reputation
of possessing
properties
fatal
to
flies
that
sip
its
juice.
This suggests
the names muscaria, Fly
amanita. Fly agaric
and Fly killer
by
which
it is known.
I have myself seen the
cap of
a
single
specimen
surrounded
by a
circle
of
lifeless
flies
that
had sipped
the viscid
juice from its
moist
surface
and
fallen
victims to
its
virulent
properties
before
leaving the
place
of their fatal
repast.
Some
have
attempted an explanation
of the
contradictory
statements
concerning this
plant
by
supposing
that
its
poisonous
properties
are
not
always
developed,
that
in some localities
or under
favorable
circumstances
it
is harm-
less.
This explanation
violates our
sense
of the constancy
of Nature,
and
is
not
at all
satisfactory.
In
the
case of my
own
correspondent,
the
caps were
peeled before
cooking.
May
it
not
be
that
much of
the
noxious
quality
resides
in the epidermis
and the
viscid
substance
upon
it,
and
that
by
discarding
this
the
dish
is
rendered
less
dangerous?
In
some
cases
it
is said
that
those
who
eat
it freely
and
without
harm
boil
it a
long time
in
water
and
throw
away
the
water.
In this
way,
doubtless,
much
of the
poison
is
abstracted.
Long
soaking
in
salt and
water,
also
in
vinegar,
have
been
recommended
as
a means
of
rendering
suspected
or
noxious
species
harmless,
and
may
have
been
prac-
ticed
in
some of
the
cases in
which
this
fungus
has
been
eaten
with
impunity.
Whatever
may
be the
explanation
of the
contradictory
statements,
the only
safe way is
to
consider
this
species
as deleterious
and
avoid
its
use under
all
circumstances.
There
is
no
need
of taking
any
risks,
with
suspected
species,
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POISONING
FROM
FUNGI
35
since
there
are
so many good
ones against
which
no
charge
of
evil
has ever
been
established.
A second
very
poisonous
species
is the
White or
Deadly Amanita
{Amanita
phalloides),
common
also
in
some
parts
of
the
United
States.
This
species
is
described
in
another
part
of
this
work.
This
and allied species are
eaten
ignorantly
by
persons
who
do
not
know
the nature
of the powerful poison
found
in
the
plant.
Prof.
Ford
says, A
small
amount
of the
fresh
material
is
sufficient
to
cause
profound illness
with fatal
outcome,
so
potent
is the
poison
contained
in
its
meshes,
and
the raw
plant
seems
usually
more toxic
than
the
cooked
specimens.
Two or
three
'deadly
amanitas'
suffice
to
bring on
disastrous
results,
and
Plowright
reports the death
of
a
child
of
twelve
from eating
a
third
of the
pileus
of
a
smjall raw
plant. The
extreme
toxicity
of
this
species
illustrates
the
dangerous
consequences
which
the admixture
of two or
three
specimens
to
a dish of
edible
mushrooms
entails.
Following
the consumption
of the fungi
there
is
a
period
of
six
to
fifteen
hours
during which
no
symptoms
of
poisoning
are
shown by the victims. This
corresponds
to
the
period of incubation
of other intoxications
or
infections.
The first
sign of trouble
is
sudden
pain
of
the greatest intetisity located in the
abdomen,
accompanied
by vomiting, thirst
and choleraic
diarrhoea
with mucous
and bloody
stools.
The latter
symptom is
by
no
means
constant.
The pain
continues
in
paroxysms
often
so severe
as
to
cause
the
peculiar
Hypocratic
facies,
la
face
vulteuse''
of
the
French,
and
though sometimes
ameliorated
in
character,
it usually recurs
with
greater
severity.
The
patients
rapidly lose
strength
and flesh,
their
complexion
assuming a peculiar
yellow tone.
After
three
to four
days
in
children and six
to
eight in adults the
victims sink into
a
profound
coma from which
they cannot
be roused
and
death
soon
ends
the
fearful
and useless tragedy. Convulsions rarely if ever,
occur
and
when
present
indicate,
I
am inclined
to
believe,
a
mixed
intoxication, specimens
of
Amanita
muscaria
being eaten with
phalloides.
The majority
of
individuals
poisoned by
the
deadly
amanita die, the mortality varying
from
60
to
100
per
cent, in
various
accidents,
but recovery
is
not
impossible
when
small
amounts
of
the fungus are
eaten, especially if
the stomach be very promptly emptied,
either
naturally or
artificially.''
Kobert
isolated from the
fungus, a
substance
which he
called
phallim,
and
which
had
the
property
of
disolving the red
blood
corpuscles. Such
substances are called
hemolysins.
Prof.
Ford
says,
''Very
minute
traces
of this
substance
brought in
contact
with the red
blood cells of man or
with those
of
animals,
produced
within
a
short
space
of time, fifteen
minutes
to
one
or
two
hours,
a
complete solution of
these
corpuscles
a
laking of
the blood.
So
powerful
was
the hemolytic
action
that even
in
a
dilution of
1-125,000
it
was
still
operative
upon the red
cells of
ox blood.
In
a
recently published
statement by
Prof. Ford it
appears
that
i
the
fungus
always
contains
another
poison
which
differs
from
hemolysin
in being resistent
to
heat
and
digestion,
the blood-laking
substance
phallin,
being destroyed by
Tieating
to
70
C,
and
by
the
action
of the
digestive
ferment.
This substance
he
called
Amanita-toxin,
and the
blood-laking
substance
Amanita-hemolysin.
Abel
and
Ford
2
have
shown that
the
so-called
phallin,
regarded
by
Kobert as
1
Science
N.
S.
30:101.
2
Jour.
Biol.
Chem.
2:273;
1907.
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MANUAL OF POISONOUS
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a
toxalbumin
is
a
glucoside.
Prof. Ford
has
obtained
an anti-poison
or
an
anti-hemolysin
with
a
high grade of immunity.
According
to
Schlesinger
and Ford
^
the
Amanita-toxin in
a
purified
state is one
of
the
most powerful
of organic
poisons
four tenths of
one
milligram
killing
a
guinea
pig
within
twenty-four
hours.
Ford
believes that
the
hemolysin
plays
no
part
in
human
intoxication, but
that the toxin is the active principal which resists
the action
of -the
gastric
juice and
boiling. He
finds
that the Amanita
rubescens
considered
an edible
species
by
some,
contains an
hemolysin
as
powerful
as the
Deadly
Amanita. He
found
a toxin
and
an hemolysin
in
Amanita virosa.
The
latter
substance
in
a
dilution of
1-200
killed a guinea
pig.
The
A.
spreta
produced
in-
toxication
and
according
to
Ford must
be
classified
with
the
deadly
poisonous
as the A. verna.
The A. strobiliformis, A. chlorinosma, A.
radicata,
and A.
porphyria,
do
not
contain hemolysins but small
quantities
of
a
toxin
probably identical
with
amanita-toxin.
The
Amanita solitaria,
regarded
as
edible,
causes the
blood
corpuscles
to
adhere
in clumps much as agglutination
occurs
with typhoid
bacilli
when
brought in contact with
the blood of
a
typhoid
patient.
1
Jour.
Biol.
Chem.
3:279,
1909,
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CHAPTER
VI
POISONING
FROM OTHER PLANTS.
EQUISBTOSIS,
LOCOISM,
AND
LUPINOSIS
Equisetosis.
It has
been
recently
proven
by
direct
experimentation
that
the common
horsetail
(Bquisetum
arvense)
when
ingested in
sufficient
amount, is capable of producing
fatal
poisoning
among
horses. This
discovery is
of
great
importance since
the plant
has a wide
distrilstrtionrand
at
times
is
the
cause of
extensive
losses.
The
common
horsetail
thrives best
in
moist
sandy soils or in
low,
damp
meadows,
which
are
not frequently
cultivated,
and
often constitutes
a large part
of
wild
hay.
The
dried plant
alone
seems
to be
poisonous. Young
horses
seem
to
be the most
susceptible.
Sheep
are
supposed
to be slightly
susceptible although
cattle eat the
hay
in which
the plant
occurs in
large
proportion,
with
impunity.
The
toxic
principle
of the
plant
has not
been
determined.
Symptoms.
The
effects
of poisoning
from
eating
horsetail
appear
at
times
varying from
two
to five weeks,
depending upon
the age of the animal,
and
the
amount
of
contaminated hay
ingested.
The
first
symptoms
are
usually
unthriftiness, general
bodily
weakness
and
emaciation.
The
animal seems
to
have
a depraved
appetite,
preferring
the
plant
to wholesome feed.
As
the
disease
progresses the
muscular
weakness
becomes more pronounced,
the animal
loses
muscular
control and
exhibits
in-
coordinate movements.
During this
stage the pulse
and
temperature are
de-
pressed, extremities are cold and the visible mucosae
are pale.
Appetite
usually
remains
good
until the
end and
consciousness is apparently
retained.
Finally
the animal falls, manifests nervous excitement, paroxysms
of convulsions appear
and death
results
from
exhaustion.
In the
final
stage
the
pulse
becomes
ac-
celerated and
the temperature elevated.
Hypostatic
pneumonia
is
a
frequent complication.
Treatment.
The
first
step
in
the treatment is the
removal
of the
cause.
A
cathartic
should
be
administered
to
rid the
bowels
of the
irritant
and
nerve
and heart
stimulants given
to
combat the symptoms
of depression. In case
the patient is
unable to
stand,
it
would
be
advisable
to give some support.
When the
animal
is
down
it
becomes
necessary
to guard against the
develop-
ment
of hypostatic pneumonia.
Where
cases
are not
too
far advanced and appropriate treatment
is
in-
stituted,
recovery
is
the
usual result.
(Stuhr).
Stock-poisoning
by
the
loco
weed is
a
frequent
and
serious
con-
Locoism.
dition with which the
stock-owners
of
the western
half of the
United
States have
to
contend. Montana
and
Colorado,
especially,
sustain
heavy annual losses. Similar
diseases
occur in
other
parts
of
the world.
In
Australia
other plants of the
order
Leguiminosae like Gastrolobium
produce
similar
symptoms.
Maiden
i
states
that the Nenta
Lessertia
disease
of
S.
Africa
is
identical
with a disease of
the Pea-eating
animals
of
Australia and
1
Misceil.
Pub.
Dept.
Agrl.
N.
S.
Wlales, 477: 11.
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38
MANUAL
OF
POISONOUS
PLANTS
with the Loco
disease
of the
United
States.
Many
forage
plants
of
excellent
repute
such
as
white
clover,
alfalfa,
lotus
and
other
plants,
may
produce
tympanites.
Fig.
8. Common
Horsetail
(Bquisetum
arvense), the
plant
causing
E)quisetosis. 1.
Fer-
tile
stems
terminating in
cones
a.
2,
Sterile
stem.
a. rhizome
tubers.
3. Sporophyl
with
sporangia.
4. Sporangia opened
to
discharge
spores.
5, 6,
7.
Spores with
spiral
elaters.
After
Wossidlo.
Symptoms: difficult breathing;
the
poison
enters
the circulation and
stops
the
action of the lungs and heart when
the
animals
stagger
and
die.
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POISONING
FROM
OTHER PLANTS
39
In the
advanced
stages the animals
become
frantic,
hence the name loco
or
crazy.
Horses
and
sheep are the
most susceptible, although
cattle
are also
affected.
Of
the
various
species
of
loco
weed,
the stemless
loco
Oxytropis
Lamberti
Pursh),
and
the
woolly
loco
weed
{Astragalus
mollisismus
Torr), are
the most
injurious.
These weeds grow
luxuriantly
on sandy ranges
and
appear
early
in
the spring when
other
vegetation
is
scarce, and
since they
retain
their fresh
Fig. 9. Loco
Weed
(Astragalus
nwllissimus)
,
U. S.
Dept.
Agrl.
green
color
during
the
entire
summer they
prove especially attractive to
stock.
Recently
the
poisoning has
been
attributed by Dr. Crawford
and others of
the
U. S.
Dept.
of
Agrl.,
to
mineral
salts
in the
plant.
The period
of
greatest
danger
is chiefly
during
the
month
of
May.
Symptoms.
The
symptoms,
which
are referable
to
the
nervous
system,
are
attributable
to
the
narcotic
eflfect
of the
plant.
They
appear
slowly
and
are
ap-
parently
divisible
into two stages.
The
first stage is
characterized by
the
follow-
ing
symptoms
: Stupor,
defective
vision